Abstract
The action of inorganic forms of selenium (Se) on blood platelet aggregation, secretion and the arachidonate pathway in vitro was studied. It was shown that sodium selenite, after 30 min preincubation, inhibited platelet aggregation induced by 0.1 U/ml of thrombin and by 10μxM ADP (about 30% inhibition of aggregation after pretreatment of platelets with 10−4 M of Se). Contrary to sodium selenite, sodium selenate did not affect the platelet aggregation induced by either agonist. Pretreatment of blood platelets with sodium selenite resulted in a statistically significant decrease in adenine nucleotide secretion (P< 0.01) and release of malonyldialdehyde (MDA), produced in equal amounts to TXA2, in thrombin-stimulated platelets (P<0.001). However, selenite did not change the level of MDA/TXA2 in sodium arachidonate-stimulated platelets. We conclude that the inhibitory effects of sodium selenite on platelet activation could be the result of decreased synthesis and release of secondary agonists (TXA2, ADP) in stimulated platelets. It is also possible that sodium selenite blocks the release of arachidonic acid from platelet membranes via phospholipases.
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